This CD274 (Atezolizumab Biosimilar) antibody is un-conjugated
Application
Flow Cytometry (FACS), In vivo Studies (in vivo)
Purpose
Atezolizumab Biosimilar, Human PD-L1 Monoclonal Antibody
Specificity
The in vivo grade atezolizumab biosimilar specifically binds to the human PDL1 protein.
Characteristics
Recombinant Humanized IgG1 Monoclonal Antibody.
Purification
Protein A affinity column
Purity
> 95% by SDS-PAGE under reducing conditions and HPLC.
Sterility
0.2 μm filtered
Endotoxin Level
< 1 EU per 1 mg of the protein by the LAL method.
Immunogen
The anti-human programmed cell death ligand 1 (PD-L1) monoclonal antibody atezolizumab biosimilar was produced in the atezolizumab biosimilar CHO stable cell line.
Research Grade
Reactivity: Human
Host: Mammalian Cells
Monoclonal
unconjugated
Recombinant Antibody
Application Notes
ELISA, neutralization, functional assays such as bioanalytical PK and ADA assays, and those assays for studying biological pathways affected by atezolizumab.
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
PBS, pH 7.4, no stabilizers or preservatives.
Preservative
Without preservative
Handling Advice
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
Storage
-20 °C
Storage Comment
12 months from date of receipt, -20 to -70°C as supplied. 1 month from date of receipt, 2 to 8°C as supplied.
What is Atezolizumab biosimilar research grade? Atezolizumab is a humanized monoclonal antibody directed against the human protein ligand PD-L1, with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab is an Fc-engineered, humanized, monoclonal antibody (IgG1κ isotype). Atezolizumab biosimilar uses the same protein sequences as the therapeutic antibody atezolizumab.
PD-L1 (B7-H1 or CD274, programmed cell death ligand 1) and PD-L2 (B2-DC or CD273, programmed cell death ligand 2) are the two ligands for the receptor PD-1 (CD279, programmed death 1). PD-L1 is an immune checkpoint molecule expressed on both tumor cells and certain immune cells. The binding of PD-L1 to its receptors PD-1 or B7.1 on activated T cells causes an inhibitory signal to suppress their production in the lymph nodes, thereby preventing immune responses to events such as pregnancy or autoimmune disease. This pathway is also utilized by cancer cells to evade the immune system through evasion of anti-tumor T-cell response. Furthermore, over-expression of PD-L1 and PD-1 has been linked to increased tumor aggressiveness and poorer prognosis. Atezolizumab binds directly and selectively to PD-L1 and blocks interaction with both PD-1 and B7.1 receptors, thus reinvigorates and enhances the body’s adaptive anti-cancer activity. Disrupting the PD-L1/B7.1 interaction may also enhance T-cell priming, which could result in increased duration of response and survival.